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Islam, Suicide Bombings, IQ and Consanguinity

1650 words

A lot of people seem to confuse causes between ‘Islam’ and behavior that’s just ‘low IQ’. Whenever these attacks like shootings, sexual assaults and rapes happen, that’s due to their low IQ; not religion. I wrote about this in IQ, Inbreeding and Clannishness. All of the behavior you see is due to low IQ. 1) being in an area with a hot climate and 2) cousin marriage has been going on there ever since Jews from the Levant introduced it to them around 200 BC. To quote myself:

Those innate behaviors which result in the favoring in all areas of life, themselves and their family, is a result of genetic similarity because of the closely related genes they share (the father’s brother’s daughter type is the most common in the Muslim world). Also, first and second cousin marriages are more common, which also result in increased altruism for their own family because of the close genetic similarity, but also those in their own group, which is mediated by the brain hormone oxytocin.

In a paper on the mean IQ of Muslims and non-Muslim countries, Donald Templer states that the Muslim world, which used to be have great intellectual achievements from the 7th to 12th centuries, has seen an underrepresentation in highly creative contributions in science journals. This is because of the inbreeding effect (2.5 to 10 point drop in IQ) of close cousin marriage. He ends up saying that genetic factors are more important than social/cultural/religious values (back to the inbreeding, causing defects and lowering IQ) in regards to IQ.

I also put a map of individualism and collectivism in Europe here. You can see that the collectivist countries are fighting back more. The countries/regions where it’s more red roughly matches up to the situation. You can see how in Central, Northern and Northwestern Europe they’re more individualistic, as well as more atheist, than those collectivist countries. So that leads to what we see with this ‘welcome refugees’ signs, as well as, I would assume, more oxytocin in the brain for Europeans, which leads to more altruism towards other peoples. Of course, 1000 years ago, the high altruism was fine due to being a mostly homogeneous society. But when others move in who are not from the area, and who do not have the same biology as you due to certain selection pressures, that’s when the ‘clash of cultures’ commences. Which it’s not really a clash of culture, more like a clash of biology, because 2 groups who shouldn’t live together are being forced to live together.

This also brings me to people who confuse the causality between Islam and blacks. As I said, it’s a low IQ religion (which I have provided enough evidence for my case). So blacks who become Muslim do so because of low IQ. Anything after that doesn’t mean that being a Muslim had them do it. Lets say that Islam never popped up and the same peoples were still there, continuing such close inbreeding, would that be Islam doing it? No. It’s their biology. **

Using environmental factors (Islam, culture) is what leftists do. In my post on behavior not equaling genes plus environment, I showed how people create their own environments based on their own genetics. The environment we put ourselves in is based on our genetics. We can clearly see that Islam is bringing their culture (genetics) to Europe and are incompatible with Europe as well as all Western societies around the world. Due to this, we can see that wherever any population goes, it will be the same from the original place they emigrated from if migration in large enough numbers occurs. A country is only as good as its majority population.

In Non-Western People are Abnormal to Our SocietiesI showed how due to differing cultures (genetics), these third-world immigrants coming into our countries cannot readily assimilate due to differing average IQs and other hormones that lead to crime differentials with the native population. Though Arabs are Caucasian, evolving closer to the equator lead to higher levels of testosterone as more exposure to the sun increases vitamin D levels, which is not a vitamin but actually a steroid hormone. These differences in testosterone then lead to more sex attacks with high testosterone combined with low IQ. Lower IQ people are less likely to be virgins than higher IQ people. This shows that higher IQ people have less testosterone and can also hold back urges more than lower IQ people. This then translates over to an increase of sexual assaults by ‘migrants’ to European women. These ‘abnormalities’, though, would be abnormal anywhere. Putting differing cultures (genetics) in a place with a completely different culture will lead to strife due to genetic distance between the two populations.

I wrote in Evolutionary Reasons for Suicide Bombings that Muslims who suicide bomb do so to increase inclusive fitness. The increase in inclusive fitness comes about due to the suicide bomber having no prospects as well as no kids, so he/she is just taking up resources. By committing suicide, they are freeing resources for others who have a better chance to spread their genes. Many suicide bombers come from middle-class backgrounds, which further proves the case for genetic interests being the cause for this. The majority of Al-Qaeda members come from educated, middle-class backgroundsEven for Palestinian suicide bombers, none of them were poor, uneducated, simple minded nor depressed.

The average IQ for a criminal is 85 adult offenders, 92 for juvenile offenders. What’s the average IQ in the Middle East? 81, around 1.3 SD lower than average, and 4 points lower for chronic adult offenders in America. The lower IQ comes from being more inbred, which then manifests itself in the crime rate. The strife in the middle east can also be traced back to IQ and consanguinity rates in those populations. How inbred a population is predicts IQ as well as how much strife occurs in those populations.

Germany has said they will begin IQ testing their ‘migrants’. If it works well (I highly doubt it will, and if it is, it won’t be implemented well) this could curb some attacks that happen. Since IQ differences between populations are one of the biggest causes for crime differentials (lower IQ is also correlated with higher testosterone) between them, screening for and only allowing high IQ ‘migrants’ in would curb some violent crime and sex attacks if implemented on a wide enough scale. IQ differences between populations are one of the biggest reasons for differences between any population you can think of.

For a comparison, we can use Christian Arabs. Christian Arabs are less inbred than Muslim Arabs, which shows in the amount of terror attacks committed by Christian Arabs, which I can’t find any data for. If anyone has found any, leave a comment. hbdchick then says this about consanguinity between Christian Arabs and Muslim Arabs:

so, the rate of cousin-marriage amongst lebanese christians was 16.5% while the rate for muslims approached double that at 29.6%.

christians married cousins more distant than first cousins at a slightly higher rate than they did first cousins: 8.6% (>1C) versus 7.9% (1C). muslims, on the other hand, favored first cousin marriage: 17.3% (1C) versus 12.3% (>1C). this is a similar pattern found elsewhere in the middle east/arab world. in egypt, for instance, copts tend to marry second cousins while muslims tend to marry first cousins (no, i can’t find the reference!).

there was also more fbd marriage amongst muslims (6.4%) versus christians (3%).

This is directly mirrored in how often we hear about Christian Arab attacks and crime (I haven’t heard of this), showing that consanguinity rates can predict crime rates. Due to this extreme inbreeding, they are more genetically similar, which leads to higher amounts of altruism for their own group, in turn leading to derogation of the out-group. Europeans are, on average, less inbred than Muslims. This is why it’s said that Muslims are incompatible with our societies. They are more clannish and altruistic for their own. Like JP Rushton said, groups will proliferate ideas that are good for their genetic interests.

Even more evidence can be shown with Chechen inbreeding. I can’t find any data on Chechen IQ, so lets use the closest country to Chechnya, which is Georgia with an average of 94. Since inbreeding can depress IQ 2.5 to 10 points, Chechnya’s average IQ should be somewhere around the mid-80s. This shows similarity with the consanguinity rate. hbdchick then concludes:

it’s no wonder, then, that they still engage in blood feuds (just like the albanians). you’d half expect them to build tower houses for protection during clan disputes like the albanians or the maniots.

oh, wait.

Muslim (Arab) populations are incompatible to Western societies due to how inbred they are. Their own societies are built on their genetics, which they then bring to the West and attempt to bring what they’re running from to their new host country.

In conclusion, whenever people say “it’s Islam doing it”, it’s low IQ behavior. Those with lower IQ are more likely to be drawn to Islam. Islam developed after 1300 years after the start of Arab inbreeding.  We can draw, from IQ from American criminals, that 85 is the sweet spot for criminality, and since criminality is correlated with low IQ more so than any other variable you can think of. A good example of this is a low IQ person coaxed into committing a crime. It’s an obvious biological difference, the sociopolitical garbage is just that, garbage. The biology drives the politics. Consanguinity rates are one of the biggest factors. You should be concerned with the biology aspect.

Note: When I say “Muslim” I mean Arab. I am also not attempting to “apologize” for terror attacks. I’m simply looking at it through the lens of evolutionary psychology. Most people who read this blog know why Africans act the way they act, and African “migrants” are no different.

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How to Use Current Knowledge to Effectively Treat the Symptoms of PWS Patients

2550 words

Abstract

Researchers have tried to manage those with Prader-Willi’s Syndrome for multiple decades. Though they have greatly curbed some of the implications of the disease, there are still numerous ways in which we can better use our knowledge of how the disease manifests in order to better help those suffering from PWS. Looking at research into how the extra chromosome 15 is linked to low IQ; IQ and its relationship to obesity; how the ability to delay gratification leads to obesity; growth hormone treatment to better treat low muscle mass and higher body fat; and finally using reinforcement theory to punish a response, where doing so will greatly diminish the probability of that response occurring again in the future; all of these factors can be used in conjunction to better mitigate problems from the disease. By examining all of these variables and thinking of better ways to handle them, we can then think of other, better ways to manage those with PWS. In doing so, we can better increase the quality of life of those suffering from PWS, as well as have less of a strain on healthcare workers who care for them. With new advances in technology with CRISPR Cas9, we can then edit the genomes and chromosomes of those suffering from this disease.

 

How to Use Current Knowledge to Effectively Treat and Manage the Symptoms of PWS Patients

How can we use the research on chromosomal differences, research on their IQ differences and their lack of ability to delay gratification that, in turn, would help those individuals with the disease?  Seventy percent of PWS cases are attributed to the deletion of chromosome 15 (Ledbetter et al, 1981). Maternal uniparental disomy, which involves receiving an extra chromosome 15 from the mother, is yet another cause of PWS (Wang, 2004).

Whittington, Holland and Webb (2009) found that there was variation between families in deletion of chromosome 15. They found that the PWS and sibling IQ correlation was .3, a modest correlation.  What was also noticed was that there were subtype differences which manifested itself in the familial differences in IQ. As they expected, the correlation with normal siblings and those with PWS was .5 in those who suffered from PWS due to unilateral disomy. But in the second subset (the chromosomal deletion subset), the correlation was negative at -0.07. Their research shows great promise in the role of chromosome 15 and IQ. They end up concluding that there needs to be an explanation for the small genetic differences between them. How can we use these differences in IQ to help people with PWS and what does this suggest for other symptoms of their disease?

Kanazawa (2014), reviewed the data on the research between obesity and IQ. What he found was that those studies that concluded that obesity causes lowered intelligence only observed cross-sectional studies. Longitudinal studies that looked into the link between obesity and intelligence found that those who had low IQs since childhood then became obese later in life and that obesity does not lead to low IQ.  The average IQ for an individual suffering from PWS is 65 (Butler, Lee and Whitman 2006, p. 13), so that is one reason they have a tendency to be obese. He states that those with IQs below 74 gained 5.19 BMI points, whereas those with IQs over above 126 gained 3.73 BMI points in 22 years, which is a statistically significant difference. Also noted, was that those at age 7 who had IQs above 125 had a 13.5 percent chance of being obese at age 51, whereas those with IQs below 74 at age 7 had a 31.9 percent chance of being obese. This data makes it clear: low IQ is correlated with obesity, so we, therefore, need to find sufficient measures to help those with lower IQs who also suffer from PWS to better maintain their good health. Since we can better identify those PWS individuals who have lower IQs based on how they got the disease, we can then show them more attention in an effort to have them manage their gratification better. Moreover, the lack of ability to delay gratification is also correlated with low IQ (Mischel, Ebbeson, and Zeiss, 1972).

Schlam et al. (2013) observed in a follow-up study to the Marshmallow Experiment that found in a longitudinal study of individuals they found forty years later from the original Marshmallow Experiment, due to inability to delay gratification forty years previously, that was one cause of becoming obese forty years later. Due to PWS sufferers having lower average IQs, and, therefore, a lack of ability to delay their gratification, this is direct evidence that those PWS sufferers with low IQs need more stringent measures to be taken on them, which would then be helpful to those individuals who have a hard time delaying their gratification, which is partially caused by the drop in IQ due to the additional chromosome 15. We can see how those with PWS act; they want their gratification now and do not want to wait for it. This is why, when unsupervised, that those with PWS gorge on the food they understand they should not have, but do so, nevertheless, since their low IQ is correlated with lack of ability to delay gratification, which manifests itself in their obesity. We clearly need to find better methods in which to help those with low ability to delay gratification, which would strongly help those suffering from PWS.

Dykens et al (1997) note that those with PWS have hyperphagia, which correlates with their insatiable want for food. They state that the lack of fullness is due to an altered function of the hypothalamus, which is the part of the brain that is in control of feelings of satiety. Certain States gave restrictions to homes that take care of those with PWS and have come under fire because of this, mainly due to human rights violations. We must ask, then, should we limit their access to food if it will prolong their lives? Will doing so inhibit their freedom to do as they choose? PWS sufferers also have coronary heart problems; one could argue that given their free ability to choose what they want to do unfettered will lead to premature death due to obesity-related complications. Does their disease truly not allow them to learn the consequences of their behavior? Do they have the intellect to really understand the consequences of their actions of consuming too much food? There is no established or known way to control those with insatiable eating habits due to hyperphagia. So would the best course of action to take with those with PWS actually be to constantly monitor them and to lock access to easily attainable food? My answer is yes, however, there is a clear fine line in whether restricting access to food and constantly monitoring those with PWS infringes on their human rights, or that doing so actually will help them live better, healthier lives since they would have the constant supervision around them to better control their out of control eating habits. When negative actions occur, one idea that can be shown to them is constant positive reinforcement so that they may be better able to understand that what they are doing is harmful to their bodies. We can then use positive reinforcement when they do reach a healthy weight, so, in turn, they will have a higher chance of keeping a healthy weight. They may reap the benefits of positive reinforcement, and stick more closely to their program, and therefore, stay healthy.

The hormone ghrelin is secreted from the hypothalamus. With an altered hypothalamus, this would cause ghrelin levels to overload; then the individual suffering from PWS would feel the need to insatiably gorge on food due to this chemical imbalance in the brain. Ghrelin increased feeding in rats and ghrelin is the physiological mediator of feeding and probably has a function in growth regulation by stimulating feeding and release of growth hormone (Nakazato et al, 2001). There is a correlation between want of food, ghrelin release and growth hormone production. By attempting to mediate these variables, those who suffer from PWS will be able to better control their eating habits through positive reinforcement and better, more sustainable habits. Since whenever we eat we get a release of ghrelin that makes us hungry, people pretty much set their own eating times by eating multiple times a day. This affects PWS patients the same way. They can’t stop eating, due in part to constantly eating which constantly releases ghrelin in their body.

PWS sufferers have low muscle tone and, conversely, more body fat. Growth hormones may be a valid way of alleviating that problem, which in turn will give them a slightly higher resting metabolic rate so that they may burn slightly more calories, in an effort to stay healthier. Growth hormone therapy is great for those with PWS though they are largely inactive and lead a sedentary lifestyle, the growth hormone will allow them to have less body fat and more muscle mass. As noted earlier in my paper, those suffering from PWS have altered function in their hypothalamus, which is also where growth hormone is secreted. Aycan and Bas (2014) state that treatment with growth hormones should be strongly considered for those with PWS.

PWS sufferers are also quick to anger, which can be correlated with their sub-average IQ. They may, for instance, become irate at the fact that they do not have constant access to food, and may turn to emotional, angry and infantile outbursts in an attempt to receive what they want. This is one way that it’s tricky to treat those with the disease. How do you tell an individual with PWS who wants something “No”? Measures should be taken to show those with the disease what they are doing to their bodies in the simplest way possible as to better get the point across to them. We can help those sufferers of PWS who are quick to anger with by allowing them to discern between right and wrong ways to handle times when they don’t get what they want with positive reinforcement.

Since those who suffer from PWS have behavioral problems, there are better measures we can take to assure that they don’t have their violent outbursts. When positive reinforcement is consistently shown to an individual who has PWS, he will have more success with his program. When they do something wrong, they can then be shown positive reinforcement, and through being shown positive things with reinforcement theory, they can better learn that certain actions they take are dangerous and shouldn’t be done again, as Rushton (1980) states: “If one rewards a response, it will increase the probability of the future occurrence of that response. If one punishes a response, it will decrease the future probability of the occurrence of that response.” (p. 90).

Discussion

In this paper, I have presented causes for PWS as well as effective ways to manage the disease. To look at how IQ affects individuals in regards to obesity and because it is highly correlated with other measures as well, we can then better help those with the disease. By seeing which individuals have the parental disomy version of PWS, we can then monitor them and give them better care because of their lowered IQ and make sure they stay at a healthy weight. One of the best measures to take is to heavily restrict food, i.e., make sure ability to access food at all hours of the day is restricted along with constant supervision. Though, there are rights groups fighting for them saying that their human rights are being infringed on. In allowing them to have free reign over what, how and when they eat, they will gorge themselves to obesity, as well as lead themselves to horrible complications that come along with increased food consumption. When one is caught consuming food he or she shouldn’t be consuming, punishing them and letting them understand that the behavior they took was wrong will lead to better choices and outcomes from those choices, due in part to the main facet of reinforcement theory, that punishing a response will lead to a reduced outcome in that response that was punished happening in the future. Also, with the advent of CRISPR Cas9, we will be able to edit genomes, and therefore, eventually, put an end to PWS. It will enable us to fix the chromosomal deletion and uniparental disomy, which will eradicate this disease.

Conclusion

There are better, more helpful ways in which to help those suffering from PWS. By identifying and attempting to correct these abnormalities, those who suffer from the disease can, therefore, have a better quality of life due in part to the extra measures taken. By understanding that their lower average IQs lead to a lot of the problems associated with the disease, we can better structure methods for them to keep on a healthy track and reinforce positive behavior through reinforcement theory. Since obesity is correlated highly with low IQ, we can, therefore, use this information to better help those who suffer from PWS that have low IQs. Locking up food instead of providing free access, as well as understanding they do not have the ability to delay gratification, would be a big start to find better ways to treat sufferers of PWS. Treating negative actions with positive reinforcement through reinforcement theory will lead to better and increased prosocial behavior. It’s been shown that if you punish a response, then it will decrease the future probability of that response occurring. The advent of CRISPR Cas9 will then allow us to edit the chromosomes of those with this disease in the future. Should we use genome editing on individuals with this disease, as well as several other chromosomal/genetic diseases? I believe we should, in doing so, we will greatly increase the quality of life of those with the disease.

 

References

Aycan, Z., & Baş, V. N. (2014). Prader-Willi Syndrome and Growth Hormone Deficiency. Journal of Clinical Research in Pediatric Endocrinology Jcrpe, 62-67.

Butler, M. G., Lee, P. D., & Whitman, B. Y. (2006). Management of Prader-Willi syndrome (3rd ed.). New York: Springer-Verlag.

Dykens, E. M., Goff, B. J., Hodapp, R. M., Davis, L., Devanzo P., Moss, F. . . King, B. (1997). Eating Themselves to Death: Have “Personal Rights” Gone Too Far in Treating People With Prader-Willi Syndrome? Mental Retardation, 35(4), 312-314.

Kanazawa, S. (2014). Intelligence and obesity. Current Opinion in Endocrinology & Diabetes and Obesity, 21(5), 339-344.

Ledbetter, D. H., Riccardi, V. M., Airhart, S. D., Strobel, R. J., Keenan, B. S., & Crawford, J. D. (1981). Deletions of Chromosome 15 as a Cause of the Prader–Willi Syndrome. New England Journal of Medicine N Engl J Med, 304(6), 325-329.

Mischel, W., Ebbesen, E. B., & Zeiss, A. R. (1972). Cognitive and attentional mechanisms in delay of gratification. Journal of Personality and Social Psychology, 21(2), 204-218.

Nakazato, M., Murakami, N., Date, Y, et al (2001). A role for ghrelin in the central regulation of feeding Nature 409, 194-198

Rushton, J. P. (1980). Altruism, socialization, and society. Englewood Cliffs, NJ: Prentice-Hall.

Schlam, T. R., Wilson, N. L., Shoda, Y., Mischel, W., & Ayduk, O. (2013). Preschoolers’ Delay of Gratification Predicts their Body Mass 30 Years Later. The Journal of Pediatrics, 162(1), 90-93.

Whittington, J., Holland, A., & Webb, T. (2009). Relationship between the IQ of people with Prader-Willi syndrome and that of their siblings: Evidence for imprinted gene effects. Journal of Intellectual Disability Research, 53(5), 411-418.

YM Wang, L Chuang, BT Wang, et al. Maternal uniparental disomy in a patient with Prader-Willi syndrome with an additional small inv dup(15) chromosome. J Formos Med Assoc, 103 (2004), pp. 943–947

White Men Can’t Jump? That’s OK; Black Men Can’t Swim

1200 words

Everyone sees how athletic blacks are, for instance in football, but why don’t blacks like swimming? Black children drown at a rate almost three times higher than white children. 70 percent of black children can’t swim, compared to 60 percent of ‘Hispanic’ children and 40 percent of white children. A combination of genetic and environmental factors are involved in this.

JP Rushton writes in Race, Evolution and Behavior (pg. 163):

Body structure differences likely account for the differential success of blacks at sporting events. Blacks are disproportionately successful in sports involving running and jumping but not at all successful at sports such as swimming. For example in the 1992 Olympic Games in Barcelona, blacks won every men’s running race. On the other hand, no black swimmer has ever qualified for the U.S. Olympic swim team. The bone density differences mentioned above may be a handicap for swimming.

Rushton noted above this paragraph that there are bone density differences between blacks and whites which have been noted at all ages and skeletal sites, remaining even after controlling for body mass. These differences even appear before birth, prenatally. Divergence in length and width of the bones in black and white fetus is followed by greater weight of black infants in comparison to white infants. These skeletal differences in weight obviously persist into adulthood, which then have implications for blacks with swimming, but give them advantages in other sports.

At the time of the writing of Race, Evolution, and Behavior in 1997, no black had ever qualified for the U.S. Olympic Swimming Team. However, Anthony Ervin became the first black swimmer to qualify for the Olympic swim team in the year 2000. The fact that it took so long for a black swimmer to make the Olympic swim team shows a genetic component.

Also contributing to this phenomenon is the fact that blacks have narrower chest cavities along with heavier skeletons (as mentioned above), this makes it harder for blacks to stay afloat and swim in the water. A smaller chest cavity brings with it less mobility while doing strokes in the water in comparison to one with a wider chest cavity.

Hochberg (2007) notes that fracture risk, particularly hip fractures, in whites is higher than for blacks in both sexes at 10.1 and 4.1 percent for white and black women respectively while the percentage is 4.3 and 3.1 percent for white and black men respectively. Other analyses of people aged 65 to 90 show 16.3 and 5.3 percent in white and black women while the percentage is 5.5 and 2.6 percent for white and black men respectively. Why do white women suffer more fractures? When women hit menopause, the drop in estrogen coincides with bone loss and osteoperosis. Moreover, in 2010, the Food Surveys Research Group published Fluid Milk Consumption in the United States, which shows women drink less milk then men, with seniors drinking less milk than all age groups (pg. 4). We can then infer from this that senior white women drink less milk, which is then another cause for more hip fractures and weaker bones. Though, there is of course a genetic component with blacks having stronger bones. However, stronger bones means heavier bones, which is a disadvantage when it comes to swimming.

Another funnier reason for blacks non-ability for swimming is that since blacks have a higher single mother rate (72 percent) they didn’t take them to the pool and teach their kids how to swim because they “didn’t want to get their hair wet”, as they put so much time in their hair. This may contribute to this slightly, but the physiological and biological differences mentioned above contribute a far greater amount of variance.

Blacks also wouldn’t be good swimmers due to them having more type II muscle fibers than type I, meaning their muscles fire off quicker and therefore tire quicker. This is why blacks are good sprinters, but would suffer in swimming events. Blacks also have a higher fat free bone density than whites, which leads to blacks not being able to float since fat floats.

For the same reasons why blacks wouldn’t be good swimmers, whites can’t jump, on average. Type II muscle fiber doesn’t allow for the explosive power needed to be able to jump as well as blacks. Even though blacks have a heavier skeletons than whites on average, they can still jump due to their muscle fiber typing. This is also why whites are underrepresented in the NBA (which is 74.4 percent black). Testosterone and musculoskeletal differences are the causes for racial differences in sports.

Whites drown more than blacks before 5 years of age, but after 5 years, more blacks drown in comparison to whites. Drowning in natural water settings was significantly higher for blacks than for whites, with blacks drowning more than whites at ages 7-8 through 17-18 years of age. Swimming pool drowning rates was also shown to be elevated for black children This data shows that after 5 years of age, blacks drown at a significantly greater amount than whites or ‘Hispanics’, which is attributed to the data above.

In our ‘post-racial society’, it’s become taboo to study, and even speak of differences so prevalent in our society, seeing as sports is a huge part of many peoples’ lives around the world. Most of the stars everyone speaks of are black. They must, subconsciously atleast, notice that these differences are there seeing the racial differences on the screen (except for baseball). Of course practice has a part in becoming elite in whatever sport is chosen, however, the best also have a higher inclination to want to do better as well as already being genetically gifted. Those who are more genetically different are, obviously, on the right side of the bell curve, thus, are extremely rare. Though, we can see these genetic disparities in racial differences in sports, with swimming being a huge tell.

It’s not just “a racist joke” that blacks can’t swim, there is biological and physical evidence that blacks, on average, have a more difficult time in the water due to difference in fat-free body mass as well as more narrow chest cavities and heavier skeletons than whites. The same reasons why blacks dominate other sports (football, soccer, boxing, basketball) is the same reason why blacks are underrepresented as swimmers: their biology. However, the trope that white men can’t jump is true as well, and also has it’s origin in genetic differences between the races.

The cause for racial disparities in drowning, as well as in swimming competitions is due considerably to genetic factors such as bone density and chest cavity narrowness. Other environmental factors include children not being taught how to swim due to them being more likely to be raised by single mothers. Bone density and heaviness also shows why blacks suffer less fractures than whites, with white women suffering from it the most. That same bone heaviness is also a reason why blacks are not good swimmers. Muscle fiber typing play a difference in racial differences in sports ability, which the races also vary in significantly. For these reasons, “White men can’t jump.” That’s OK, because “Black men can’t swim.”

Transvestic Disorder and Gender Dysphoria Identification and Prevention

2150 words

Abstract

Transvestic Disorder comes about in early childhood and manifests itself in sexually deviant actions. Men suffering from TD who aren’t homosexual, more likely than not, show attraction to themselves dressed in women’s clothing. The signs of TD are noticed at an early age when the individual begins to cross dress. TD is also correlated highly with numerous sexually deviant actions. Fluoxetine and serotonin reuptake blockers may be able to lessen TD since it is an impulsive disorder. With TD being co-morbid with OCD, by treating OCD we can better treat TD itself and give a better quality of life to the patient suffering from the disease. Since autogynephilia and transgenderism are related, measures taken to alleviate TD and autogynephilia could be taken to alleviate symptoms of gender dysphoria, since autogynephilia leads to transgenderism.

 

Transvestic Disorder and Gender Dysphoria Identification and Prevention

            Transvestic disorder is a paraphilic disorder, classified by the American Psychological Association (2013), in which males dress up as women to gain sexual gratification. The individual suffering from TD suffers from compulsions to want to dress as a woman, which causes distress due to the individual not wanting their secret to come out. This then leads to the quality of life of the individual to decrease due to constantly being worried about his secret coming out. TD is diagnosed when a male has sexual feelings and gets sexual arousal from dressing in women’s clothing. It is only diagnosed when these activities are ongoing for at least six months. TD is also similar to another paraphilic disorder called ‘autogynephilia’ (Lawrence, 2011), in which the subject is aroused at the thought of himself being a female, so he, therefore, then begins to dress as a woman to fulfill his sexual desires. Blanchard (1989) proposed that most gender-dysphoric males who do not show sexual arousal to men, instead show sexual arousal to themselves dressed in the opposite sex’s clothing. He concludes that the hypothesis is supported that major types of those men who cross-dress are nonhomosexual, and do so because they become aroused at the thought of dressing as a woman. The DSM V says that autogynephilia is a specifier to transvestic disorder. This is because they are characterized by the same things (American Psychological Association, 2013).

The signs of TD are noticed at very early ages. Most notable are when children begin to cross-dress at or before puberty. This then continues into their adult lives where it begins to be a problem and cause dysfunction due to needing to keep their secret. Dr. Mark Griffiths (2012) states that all though children may engage in transvestic behavior, what differentiates it between an adult suffering from TD is that the child who cross-dresses does so for excitement and pleasure, not for sexual pleasure. Though some researchers say that the disorder is brought on through childhood trauma, i.e., accidental exposure to women’s clothing or exposure to a woman who is undressing. Numerous studies have also concluded that many men who suffer from TD have had to deal with parental separation during childhood.

The American Psychological Association (2013), reports that fewer than 3 percent of males are characterized as having transvestic disorder. TD is most always seen in males, though Moser (2009) noted that in his study using the Autogynephilia Scale for Women (ASW), that out of the 29 respondents that sent back questionnaires, 90 percent would be classified as having autogynephilia. Though, by using a more meticulous definition, only 28 percent were seen to be autogynephilic (Moser, 2009).

Langstrom and Zucker (2005) observed in a sample of 2,450 18 to 60-year-olds in Sweden that transvestic disorder was correlated significantly with being separated from their parents, homosexual relations, higher masturbatory frequency, being easily aroused sexually and pornography use. Also noticed, was a positive attitude in regards to sexual arousal from pain, exposing oneself to a stranger and voyeurism were all positively correlated with TD. Langstrom and Zucker observed how TD is co-morbid with many other paraphilic disorders as well as other deviant behavior. By attempting to treat what TD is correlated with, symptoms of TD can be lessened.

Men suffering from TD and autogynephilia are told that women are the standard of beauty. They then look at themselves in the mirror and see a male and not the standard of beauty they were told of growing up. They then turn to cross-dressing to finally see their “beauty standard” in the mirror but keep it a secret. This strong want to keep their disorder a secret then leads to dysfunction. Men suffering from TD will go to any lengths to hide their secret. This then causes extreme dysfunction in their lives, which leads to a lessened quality of life.

Less than three percent of males suffer from TD in the American population, as such, it is classified as a deviant lifestyle as it deviates from the norm of the population. It causes distress due to them not wanting their secret to be discovered. This, in turn, leads to dysfunction where the individual cannot live their daily lives to the fullest due to their abnormal disorder. It finally leads to danger due to their secret beginning to consume their lives so that they’re not discovered.

There are ways to treat TD. Usmani et al (2012) follow a case study in which a 17-year-old Indian male who had occurring desires to wear his mother’s clothes. He then would masturbate in his mother’s clothes to alleviate himself. This continued on for two years so he could pleasure himself. He was caught by his parents wearing his mother’s clothes and was beaten by them for it. He then said that it is a compulsive behavior and cannot be helped. This case also shows the obsessive compulsive side to TD. They have an urge so strong they cannot help but to do it compulsively to alleviate their sexual desires. He also said that the occurring thoughts then affected his schoolwork as he was so preoccupied with the thought of wearing women’s clothes. All of his brain scans were found to be normal, so what brought on this case in the individual in the case study? He was then diagnosed with TD and prescribed fluoxetine, an antidepressant SSRI. The dose was started at 20 mg and increased by 40 mg once a day for two weeks. In his six-month follow-up, he reported lessened desire to masturbate with women’s clothes (Usmani et al, 2012).

Paraphilias and other related disorders have been thought of as sexual addictions. Though it has been argued that they are not sexual addictions, but are sexual compulsions (Stein et al, S 1992). The researchers reviewed 13 patients who showed signs of TD and were administered serotonin reuptake blockers.  The symptoms of those individuals were then divided into paraphilias, non-paraphilic sexual addictions, and sexual addictions. Stein et al discovered that paraphilias had the least improvement with the reuptake blockers whereas sexual compulsions showed the best improvement. They end up concluding that paraphilias and other related disorders are on the impulsive end of the spectrum compared to the compulsive end. These impulsions, then, have those men suffering from TD have the urge to dress in women’s clothes to fulfill their sexual impulsion.

TD is co-morbid with obsessive compulsive disorder (Abdo, Hounie, de Tubino Scanavino, and Miguel, 2001). They used longitudinal case studies in which they assessed two individuals who had OCD as well as TD. They conclude that some cases of TD may be OCD related and not always be caused by gender dysphoria. Since OCD and TD are co-morbid, by treating symptoms of OCD, the want to cross-dress will lessen, which will then lessen the symptoms of TD. Treatments could include SSRI and fluoxetine, as previously stated in the paper. Other treatment for TD should be looked at, such as treatment for OCD due to the co-morbidity between the two. By doing so, feelings of wanting to cross-dress may lessen due to one of the underlying causes (OCD) of TD being treated.

Autogynephlia could also explain transgenderism.Transvestism can be called both a paraphila and a sexual orientation. Lawrence (2004) says that it can explain mid-life MtF transitions, progression from transvestism to transgenderism, the prevalence of other paraphilias among MtF transsexuals and the late development of male intrest in MtF transsexuals. However, when Lawrence says that “Hormone therapy and sex reassignment surgery can be effective treatments in autogynephilic transsexualism”, that is incorrect. The prevalence of suicide attempts among transgenders is 41 percent according to the Williams Institute, UCLA School of Law, in comparison to 4.6 percent for the average population. That’s almost ten times higher than the national average. Clearly, surgery doesn’t do anything to alleviate the feelings of gender dysphoria, and as shown in this paper, therapy and drugs like Prozac can better help to alleviate feelings of gender dysphora in transsexuals due to them being extremely similar to eachother. These two disorders greatly mirror each other. Since Lawrence (2004) observed that there is a progression from transvestism to transgenderism, using similar techniques that work on those with TD may also work on those with gender dysphoria.

 

Discussion

TD can be helped with the correct therapy as well as right medication. With those, impulsions to wear women’s clothes, as well as impulsions to commit abnormal acts will be greatly lessened and quality of life will be restored to a somewhat normal level. Due to co-morbidity between TD and OCD, treating OCD will, in turn, better help the patient suffering from TD. When more studies are carried out on those suffering from TD, we can see whether or not SSRI drugs and fluoxetine will have the desired effect in alleviation of the symptoms of TD. The individual in the Usmani study reported lessened symptoms and impulsions of cross-dressing, so by identifying which parts of the brain are and were activated during the fluoxetine therapy, we can then better give better care and treatment to those suffering from TD. We can also use some data from TD cases for transgenders, as TD and transgenders have a lot of things in common. With therapy as well as, maybe even fluoxetine (which is just Prozac), and high doses of testosterone/estrogen, this could possibly help to alleviate ‘gender dysphoria’. It could also lower the suicide rate as it’s completely possible that these interventions could fix them mentally.

 

Conclusion

There is little current literature in treating TD, due to it being a shameful disorder and many men not speaking about what they suffer from. One major way in which to help those with TD is to administer SSRI drugs, in which compulsion to cross-dress, and other attitudes associated with TD lessened. Blanchard (1989) proposed the autogynephilia theory for those transgenders who are not attracted to men. With the obseration by Lawrence (2004) on how autogynephilia and transgenderism are related, this can better help those with transgenderism, as they can get correct help and the right hormones they need, instead of the opposite hormones. SSRI therapy is a good candidate in treating TD, as drastic changes in deviant behavior are seen while the patient is taking the SSRI drug. Seeing as most cases of TD begin in childhood before puberty, by better identifying warning signs of these disorder, we can better treat those children who are at risk of developing these disorders before they become a big problem later in life. As more men come out and say that they suffer from these disorders, more studies can be carried out that corroborate the findings in the studies laid out here. It is extremely promising that these disorders can be treated with common drugs already on the market. In those individuals suffering from TD as well as OCD, by treating the OCD first (which may be an underlying cause) the symptoms of TD may be lessened and the individual may eventually have the ability to lead a life without TD. In using these measures on those with transgenderism, this could possibly alleviate suicide rates and other negative variables associated with these paraphilic disorders and sexual orientations.

 

References

Abdo, C.H.N., Hounie, A., de Tubino Scanavino, M., & Miguel, E.C. (2001). OCD and transvestism: Is there a relationship?. ACTA Psychiatrica Scandinavica, 103(6

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: American Psychiatric Publishing.

Blanchard, R. (1989). The Concept of Autogynephilia and the Typology of Male Gender Dysphoria. The Journal of Nervous and Mental Disease, 177(10), 616-623. doi:10.1097/00005053-198910000-00004

Griffiths, M. (2012, February 28) Dressed to thrill? A brief overview of transvestic fetishism. Retrieved from https://drmarkgriffiths.wordpress.com/2012/02/28/dressed-to-thrill-a-brief-overview-of-transvestic-fetishism/

Lawrence AA . Autogynephilia: An Underappreciated Paraphilia . In: Balon R, Hrsg . Sexual Dysfunction: Beyond the Brain-Body Connection. Adv Psychosom Med 2011 ; 135 – 148

Långström, N., & Zucker, K. J. (2005). Transvestic fetishism in the general population: Prevalence and correlates. Journal of Sex and Marital Therapy, 31, 87–95

Moser, C. (2009). Autogynephilia in Women. Journal of Homosexuality, 56(5), 539-547. doi:10.1080/00918360903005212

Stein DJ, Hollander E, Anthony DT, Schneier FR, Fallon BA, Liebowitz MR, Klein DF: Serotonergic medications for sexual obsessions, sexual addictions, and paraphilias. J Clin Psychiatry 1992; 53:267–271

Usmani et al, (2012) Treatment of Transvestic Fetishism With Fluoxetine: A Case Report. Iran J Psychiatry Behav Sci. 2012 Autumn-Winter; 6(2): 100–101

 

Human Intelligence, Child Rearing and r/K Selection Theory

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In a paper titled Extraordinary intelligence and the care of infantsPiantadosi and Kidd (2016) add to the other hypotheses of higher cognition in humans (Cold Winter Theory and farming) by positing higher cognition evolved to better take care of offspring.

Their theory is that big brained parents have big brained children, with the big brained children needing to be born earlier as their head has to be small enough to pass through the birth canal. A lot of animals can stand up immediately after birth, when humans can’t even hold their head up (I will return to this point later). Human babies are born less mature than other primates, which means they are more vulnerable, thus higher cognition evolved to better care for children. All of the variables coalesce into the need for more intelligent parents, which lead to humans growing more intelligent as a result of this.

They found that weaning time, which acts as a measure of the prematurity of infants, was a much better sign of a primate’s intelligence than any other variable they looked at, including brain size.  Piantadosi said “One of the motivating puzzles of our research was thinking about those theories and trying to see why they predict specifically that primates or mammals should become so intelligent, instead of other species that faced similar pressures.”

The researchers also state that this may explain how humans developed good social reasoning and the “theory of mind” which is the ability to anticipate the needs of others as well as recognizing that other’s needs may not be the same as their own. Kidd also says how the theory of mind is especially helpful since human babies won’t talk for a couple of years. Since women took care of the children, they had to evolve a higher verbal IQ to better care for them. Along with being better able to care for children, men had to evolve high intelligence to care for both the children and women as well as hunt for food and defend his family and other co-ethnics.

Piantadosi and Kidd’s (2016) data shows that the helplessness of a primate’s newborns predict their intelligence, as well as accounting for human uniqueness in intelligence and why this level of cognition took so long to evolve. They also show how dinosaurs, who evolved in the same conditions and had a longer time to do so, did not evolve the same level of super intelligence as primates did. They also matured in eggs, showing that there is no link between intelligence and infant immarurity and birth. Humans also mature slower and need longer parental care. Due to these pressures, a bigger brain evolved. Babies are born earlier and mature slower than other animals, leading to higher intelligence. This also shows how human intelligence is so different from our closest primate ancestors.

This theory compliments the cold winters theory as well as Cochran and Harpending’s argument that higher intelligence evolved due to the advent of farming. Adequate nutrition lead to the development of higher intelligence and bigger brains as well. It also compliments other theories, including that we evolved higher intelligence due to social reasoning and reproductive pressures (sexual selection).

This theory also shows more evidence for Rushton’s Differential-K Theory. As the researchers noted, babies were born less mature than other primates babies. We can also apply r/K selection theory to this as well. Black babies are born one week earlier than white babies who are born one week earlier than Asian babies. Despite black babies being born one week earlier than white babies, black babies can support their heads at 24 hours earlier than white babies. For Asians it’s unknown, as Rushton notes in Race, Evolution, and Behavior (pg. 148). Asian children are slower to develop than white children who are slower to develop than black children, with Asian children having the biggest brains of the three races. This theory of Piantadosi and Kidd (2016) perfectly compliments Rushton’s r/K selection theory. Asians are born one week earlier than whites who are born one week earlier than blacks, which correlates with the average intelligence scores of the three races.

The cold winters theory also shows another reason for bigger brains, as those who evolved in colder climates evolved bigger brains, and therefore higher intellect. The more intelligent parents who could provide more for their offspring prevailed over those less intelligent who could not survive. This lead to more mutations developing in those with high IQ alleles making higher intelligence more prevalent in those populations who evolved further away from the equator, as well as having an adequate population for more births to occur leading to more genetic mutations which leads to higher intelligence. Since those with higher intelligence can survive more efficiently than those with lower intellect, they were able to spread their genes more by having more offspring than those with low IQ alleles (the opposite of what is happening today).

As noted previously from Rushton’s data, those with higher intelligence are born earlier and mature slower than those with lower intelligence. Black children being able to, for instance, lift their head at 24 hours sooner than white children, along with all of Rushton’s data that shows that blacks mature the fastest on all variables. Black children have to mature faster due to a higher mortality rate, which is correlated with low IQ. This is also why black girls have an earlier menarche than white girls. Since black children are born with smaller heads, they, according to Piantadosi and Kidd’s data, have lower intelligence as a result. Black children average smaller brains than white children who averahe smaller brains (and heads) than Asian children. This shows with how Asians are born one week earlier than whites who are born one week earlier than blacks.

This study shows how r/K selection theory is not dead, nor is it not a theory to take seriously, as other researchers have stated since Rushton applied it to race, since it is shown to have good predicitive power. Piantadosi and Kidd’s data corrobarates Rushton’s findings on earlier births between the races, vindicating Rushton and his r/K selection theory. Piantadosi and Kidd show that a) helpless children need intelligent parents, b) intelligent parents must have large brains and c) large brains necessitate having helpless children. This would show, in accordance with r/K selection theory that a) helpless Eurasian children need more intelligent parents, b) Eurasian parents must have large brains and c) large brains nescisstate having helpless Eurasian children.

Piantadosi and Kidd’s theory compliments other theories of human intelligence, which strengthens the cold winters theory of intelligence more, as those with higher intellect have bigger brains, and are therefore born earlier than those with lower intellect and smaller brains. As time goes on, more and more researchers will, unknowingly to them, corroborate more and more of Rushton’s r/K Life History variables. As noted by E.O. Wilson (co-founder of r/K selection theory) in defense of Rushton in the early 90s:

“I think Phil is an honest and capable researcher. The basic reasoning by Rushton is solid evolutionary reasoning; that is, it is logically sound. If he had seen some apparent geographic variation for a non-human species – a species of sparrow or sparrow hawk, for example – no one would have batted an eye. … when it comes to [human] racial differences, especially in the inflamed situation in this country, special safeguards and conventions need to be developed.

As we understand human development more, Rushton’s r/K Life History Theory will be corrobarted. This three-way pattern Rushton noticed, “Rushton’s Rule of Three“, has been corroborated yet again by other researchers. As time goes on, the true nature of humanity, as well as human races, will be revealed unbeknownst to them.

I wonder if Piantadosi and Kidd realize that they have just corroborated one of Rushton’s theories?

Polar Bears, Inuits, Evolution and Fst

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The Daily Stormer published an article today that claimed that “Polar bears are miscegenating with grizzly bears“. When polar bears and grizzly bears mate, they produce a “pizzly bear“. Due to this, the polar bear population is shrinking and the grizzly bear population is growing.

Scientists say this doesn’t look good for the polar bears; though these hybridizations are not due to ‘climate change’, as is suggested. Using a computer model, the researchers generated a prediction of the Earth’s climate from 2071 to 2100. The model analyzed how different species of birds, mammals and amphibians would need to migrate to find new territory. Birds had the highest overlap with 11.6 percent, attributed to their range from flying. Mammals and amphibians were 4.4 and 3.6 percent likely to encounter a hybridization event. Overall, about 6.4 percent of all species are expected to come into contact to even have the chance to hybridize with other compatible species. Meaning, the polar bear is not in danger of ‘dying out’ due to ‘miscegenation’.

What is missed in the article mentioned at the beginning is that polar bears and grizzly bears are even able to produce offspring at all. This is due to the two splitting around 350 kya to 6 million years ago. This article then says something vaguely familiar:

After beginning to branch off from brown bears, the polar bear’s ancestors under went a series of evolutionary changes in order to survive in the Arctic. The bears adapted to a life of hunting seals and surviving extreme cold. One of the most remarkable adaptations was the ability to thrive on a fat-rich diet withoutapparent heart damage.  (sounds like the Inuit or other Eskimo tribes; emphasis theirs)

‘The bears’ could be switched to ‘the Eskimoes’ or ‘The Inuit’and make complete sense. The Inuit also live off a high-fat diet. The higher n-3 gives immunity and boosts in health to a slew of diseases as well.

The Inuit and their ancestors evolved special genetic mutations that allowed them to partly counteract the effect of a diet high in fat. Nearly 100 percent of the Inuit have these genes, while 2 percent of Europeans and 15 percent of Han Chinese do, which means that they synthesize n-3 differently than the Inuit. Over time eating a diet high in fats, the Inuit evolved these genetic adaptions to better adapt to their environment. The genes they have also lower LDL (bad) cholesterol and fasted insulin levels, which presumably has an effect on cardiovascular disease and diabetes. This used to be the case, but “exposure to a more Western lifestyle” has made Diabetes Mellitus in the Inuits comparable to that of the general population. Since growth is reliant on a person’s whole fatty acid profile, the Inuits are, as a result of these mutations, 1 inch shorter than they should be. The same mutations causing shorter height in the Inuit have also been found in Europeans. Researchers have found many genes responsible for height, but this was “one of the strongest effects ever found by geneticists”.

These genetic mutations are around 20,000 years old and originate with their Siberian ancestors. They think that the adaptation came about in the last Ice Age, but the selection is far stronger in the Inuit, due to them being one of the furthest populations away from the equator.The researchers have also found that the Inuits have another common mutation in their population that is involved in the differentiation of brown, subcutaneous fat cells and brite fat cells. Brite fat cells burn fat for more heat, showing another adaptation they had from their diet and direct environment. This helped them survive the harsh climate.

A strict Inuit diet shows evolution in action, that populations forced to subsist mostly on one type of food/macronutrient can and will adapt to their environment over time, proving that evolution exists. However, you cannot infer from the Inuits that the effect they gain from this diet will carry over to the general population.

The Science Daily article then goes on to say people have asked themselves whether they “Should be on a Stone Age diet”. My answer to that is a resounding “No” if you think the diet will do anything different from any other diet and weight training. As stated in the SD article, you cannot say that other populations, for instance, evolved to eat a certain way cannot be made as the Inuit have certain genetic mutations that no other populations have, in the frequency they do, for that matter.

The DS article, more interestingly, doesn’t bring up how two different species are interbreeding. Humans have a Fst distance of less than .5. The Fst for polar and grizzly bears is 0.2688. Two differing populations separated anywhere between 350 kya to 6 million years ago, can interbreed, and so can humans. Sewall Wright, the creator of the Fst concept, has said that if this differentiation was noticed in any other species, that they would be noted as distinct subgroups. When it comes to human genetics and science, science chooses to take the “egalitarian route” and deny the existence of race. However, when it comes to polar and grizzly bears, talking about how polar bears are a subspecies of grizzly bears and the polar bears adapted to the cold leading to physical and physiological differences, this is fine. Just like when Rushton proposed Differential-K Theory, which is the application of r/K selection theory to humans, it got shot down, despite E.O. Wilson who co-founded r/K selection theory stating “I think Phil is an honest and capable researcher. The basic reasoning by Rushton is solid evolutionary reasoning; that is, it is logically sound. If he had seen some apparent geographic variation for a non-human species – a species of sparrow or sparrow hawk, for example – no one would have batted an eye. … when it comes to [human] racial differences, especially in the inflamed situation in this country, special safeguards and conventions need to be developed.”  Rushton’s main thesis has also never been refuted. No other explanation can fully explain the variables Rushton describes in Race, Evolution, and Behavior like r/K selction theory does.

Polar bears are not going away, and if they were, it’d just be evolution in action as the point of life is to breed and carry on your lineage (however, fitness is increased for the grizzly bear as he is gaining more habitat, yet decreasing for the polar bear due to a warming planet). The strongest populations get selected for, while the weakest become absorbed/wiped out. Since the planet is warming, as well as the grizzly bears looking for more environment some, not all, are mating with polar bears. This does not mean that polar bears will go extinct due to inbreeding with grizzly bears. Inuits are proof of the existence of evolution with how they adapted to their high-fat diet and cold environment, but you cannot use this information on their diet and say that the benefits from a high fat diet would be the same in other populations.

 

Even More Evidence for GST: Speed Daters Match on Genotype

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Your success at speed-dating might be influenced by your genetic make-up and your potential partner’s ability to detect so-called ‘good genes.’ The research team found that participants who were more likely to be asked on a second date had genotypes consistent with personal traits that people often desire in a romantic partner.

Science Daily: Your gender-stereotypic genes may be giving you a leg up in dating Researchers use a real-life speed-dating scenario to test how genetics influence mate selection

Coming off of a successful refutation of JayMan (check comments too), more evidence for our claim came out the other day. Us humans can match on genotype, which we, of course, match with people with other similar heritable characteristics. Since humans match on these traits that are more heritable than the ones that are more influenced by environment, then we can say that we are seeking out partners who are like us, therefore matching on genetic similarity.

Wu, et al (2016) examined 262 Asian Americans in a speed-dating setting. The researchers predicted that there would be considerable matching by genotype between the genders. They found that the gene A118G, which is linked to submissiveness and social sensitivity, whereas for the men, the minor variant with the -1438 A/G allele, which is linked to social dominance and leadership, were shown to have greater success. They also discovered that men and women with genotypes consistent with “prevailing gender norms were more likely to receive second date offers”

The researchers say that “These results suggest that personal attributes corresponding to A118G and −1438 A/G can be detected in brief social interactions, and that having a specific genetic variant or not plays a tangible role in dating success,” Those with the A118G polymorphism had greater capacity for experiencing social pleasure and pain as well as their need to have social contact. This also shows how  Men and women with the opposite of each allele (men having the A118G allele and women having the -1438 A/G allele) were seen as less desirable mates, showing good evidence that each allele is gender-specific. Wu also believes this effect could also expand to other social interactions, such as job interviews.

This study shows more evidence for Rushton’s theory of spouses matching phenotypically by genotype. Spouses are as similar as 4th cousins. Spousal genetic similarity is a significant driving force for human civilization, as it selected for certain traits over others that then lead to things such as higher IQ in Eurasian men to beauty in Eurasian women, vice versa for Africans. In Eurasian societies, men hunted and while women took care of the children. Higher intelligence then evolved in men due to needing to strategize, among other things such as surviving the frigid temperatures. Women took care of the children, and thus developed a higher verbal IQ as a result of this. In Africa, women gathered food, selecting them for slightly higher intelligence than their male counterparts. Conversely, the African males were selected for attractiveness (Fuerle, 2008).

Those K-selected have lower birth rates, and thus, must be more rigorous in choosing a mate. Choosing a mate based on intelligence showed that the male could provide food as well as protect the family against predators and other bands of humans. R selected humans have more children and show less care, so they have higher birth rates to counter this. They are less rigorous in mate selection due to need to have more children due to a higher death rate. This is mirrored still, even today in modern society. Human sexual selection is one of the reasons why human evolution progressed to the point is has, with the driver being evolution in harsher climates. Eurasian women needed to be more stringent in choosing mates due to a higher chance of death in choosing the wrong mate. Over time, this lead to a ‘genotype sensor’ if you will, which by matching by certain phenotypic traits (facial symmetry, skin color, height, health, etc), chances for intelligent children, better care and more food will come as a result of this stringent selection by women, which in turn lead to evolution of certain traits in Eurasian men and women.

This shows that these human differences in how we select our spouses to how our civilizations ultimately end up is due to a) climate, b) sexual selection and c) genetics. Passing on the best genes lead to an ultimately better society, and as a result, this lead to those genes that were more successful having a chance to produce more copies of themselves, assuring that society would be run well in the future. This is also why government systems such as monarchies have hereditary rulers.

I have said numerous times that the tendency to favor co-ethnics is the tendency to favor shared genes. Benefiting those similar to yourself ensures that you’re benefiting copies of your genes, ensuring your genetic legacy for the future.  Matching with those who appear similar to us by genotype when there is such phenotypic similarity shows that this is a trait we humans have to seek out those co-ethnics genetically similar to ourselves.

The Black-White IQ Gap

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(This goes along with my refutation of Steele here: Strong Evidence, Strong Argument: Race IQ and Adoption)

There is a 15 point, 1 standard deviation between black and white IQs. I will argue that they are not biased towards any group, as well as there being both positive and negative life outcomes based on IQ, crime included. This is due to false ideas of equality, some “blank slate” idea that we all have the same capacity for cognitive ability, athletic ability and so on. These egalitarian ideas, in turn, have devastating effects on our society, as we a) deny the reality of intelligence and b) deny any type of racial gaps in intelligence.

The famous words “Compensatory education has been tried and has apparently failed” in Jensen’s paper in the Harvard Educational Review that reignited the firestorm on the race/IQ debate called How Much Can We Boost IQ and Scholastic Achievement? is the reason why this debate got thrown back into the public eye (Jensen, 1969). It will be argued in this paper that he was correct and that his main thesis that blacks need differing education than do whites is correct and needs to be done.

IQ tests were first developed off of Army Aptitude Tests in the early 1900s by French psychologist Alfred Binet. They were originally used to identify at-risk populations in terms of who is mentally retarded. People then say that due to this, that IQ tests don’t test anything of worth due to the reason why they were originally developed.

In 1976, a study was conducted called the Minnesota Transracial Adoption study where they took children of different races who were adopted into different families and tested their IQs at age 7 and again at age 17. A follow-up study was published in 1992. What was found, was that IQs of transracially adopted children didn’t differ at all from children raised by their biological parents in the same area.

Dr. David Duke states in his book My Awakening: A Path to Racial Understanding (1998), that the authors waited about 4 years to publish these findings. This, of course, has to do with the political climate of today. Any allegations of “racism” can and most likely will end someone’s career; so most individuals just go the politically correct route to play it safe and keep their credentials. Blacks raised in white families hardly did any better than blacks raised in black families. If the differences supposedly were environmental in the way environmentalists say it is, how come blacks raised in rich white families didn’t reach the IQ of whites if “IQ is malleable by the immediate environment?” Because the differences are genetic.

Though, there are other studies that state that environment matters more than genetic factors. These three studies (Moore 1986; Eyferth 1961; and Tizard, 1972) all conclude that the black-white IQ gap is environmental in nature.

A study was conducted that compared IQ scores of 23 7 to 10-year-old black children raised by middle-class white families and the same number of black children but raised in black families (normal adoption) (Moore, 1986). The findings indicated that traditionally adopted black children raised by black parents had normal IQ scores (85), whereas those black children who were adopted by white families had IQs 1 standard deviation (100) above the black mean. Moore states that multivariate analysis indicates that the behaviors of black and white mothers were different in regards to how the black children were treated. She states that white adoptive mothers reduced stress by joking, laughing, and grinning. Whereas black adoptive mothers reduced stress in less positive ways including coughing, scowling and frowning. She also says that white adoptive mothers gave more positive reinforcement to their adoptive child’s problem solving whereas black adoptive mothers gave less (as I am arguing here, these traits are mostly genetic in origin, driven by IQ). She concludes that the ethnicity of the rearing environment exerts a significant influence on intellectual ability as well as standardized test scores. The sample sizes, however, are extremely small and to infer that the black-white IQ gap is environmental in origin because of a study with a small sample size is intellectually dishonest.

One study conducted in Germany in 1959 observed IQ scores of out-of-wedlock children fathered by US soldiers stationed in Germany during WWII and reared by white German mothers (Eyferth, 1961). Mean IQ scores for 83 white children and 97 mixed-race children were 97, 97.2 for the whites and 96.6 for the mixed-race children (Rushton and Jensen, pg. 261). However, these results are disputed. One, the children were extremely young, one-third of the children in the study were between the ages of 5 and 10 whereas the remaining two-thirds of the children were between the ages of 10 and 13. The malleability of intelligence is very well-known in regards to children. The heritability of IQ at age increases with age (a phenomenon known as ‘the Wilson Effect’), which Arthur Jensen states that as a child ages, social environment can increase IQ (as heritability for children aged 5 is 22 percent and children aged 7 at 40 percent). Though, as the child ages, genes activate, and they fall to their genetic potential, with genetic effects accounting for a lion’s share of intelligence (80 to 90 percent) and environment having no effect. Second, 20 to 25 percent of the ‘black’ fathers were French North Africans (Caucasians). This shows why the mixed-race children had higher IQs in the sample: about a quarter of the sample was Caucasian (Rushton and Jensen, pg. 261). Finally, rigorous selection was done on both the white and black soldiers. With 3 percent of whites getting rejected compared to 30 percent of blacks, it is shown that high IQ blacks were selected for, therefore, skewing the sample.

Yet another study on black and white children observed 2 to 5-year-olds in a nursery setting (Tizard, 1972). The white and black children both had IQs at 102.6 and 106.3 respectively. She found no significant gap in the three groups tested (white, black and West Indian). However, she did note that the single significant difference was in that of non-white children.

All three of the above studies that get cited ad nauseum have something in common: they did not retest the children again at age 17 like was done in the Minnesota Transracial Adoption Study. This is very critical. As it was alluded to earlier, as children mature, genetics exerts more of an effect than does socialization. Any IQ differences that are brought about by socialization will be mediated by genetics at adulthood, falling to the racial mean. It also noted how the age of adoption does not influence children’s IQ scores after age 7 (Jensen 1998b). This is due to, again, genetic effects being heightened as age increases.

What the Minnesota Transracial Adoption Study (Weinberg, Scarr, and Waldman, 1992) and the Eyferth study (1961) had observed was that the children born to a white mother and a black father had statistically significant differences in IQ in comparison to those birthed by a black mother and white father. This is attributed to prenatal environment. It was observed that mothers who had higher IQs and were more educated (which both correlate highly with each other), had children which, in turn, had higher IQ scores as well (Erikson, 2013). The results of the study suggest that mothers who are more educated have children who have higher intelligence. This should end this debate right there. Since, clearly, a white mother is more conducive to foster a higher IQ than is a black mother, this shows that racial differences in IQ are largely genetic in origin.

The black-white IQ gap has been noticed for over 100 years, ever since the test has been first conceptualized. Egalitarians may say that “they’re biased against minorities” or “they don’t learn the right things on the test”, all of these are easily refutable. This was true in the 70s, according to Herrnstein and Murray, but today there is no bias of that magnitude on these tests of cognitive ability.

Jensen states that genetic and cultural factors influence the black-white IQ gap the same as individual factors (80 percent genetic factors, 20 percent environmental). Since both individual differences in IQ, as well as the mean difference in the black-white IQ gap are genetic, this shows that some individuals are genetically predisposed to have lower IQs. Moreover, a multitude of traits in life fall on a bell curve, you will have some individuals at one end, and others at the opposite end, but you’ll see a majority fall in the middle of the racial mean (85 for blacks, 100 for whites, 104 for East Asians and 107 for Ashkenazi Jews). So, with equalized environments, the gap can be closed by around 3 points, but still a lion’s share of the gap is still there, which again gives credence to the genetic hypothesis.

Those who disbelieve the validity of IQ tests at the individual level, as well as the between-group level, say that test biases are the cause for lower scores in certain individuals in minority populations. Gottfredson et al state in their publication that was released after the controversial book The Bell Curve, Mainstream Science on Intelligence, that if you speak the language, IQ tests are not biased. If you don’t speak the language, you then get a special IQ test that is culture free, based on pattern recognition called Raven’s Progressive Matrices. Even then on these culture-free, word-free IQ tests, there is still a one SD gap, 15 points, between blacks and whites.

People have tried to bridge the gap, even going so far to make a test that’s ‘culture fair’ to blacks called the B.I.T.C.H. (Black Intelligence Test of Cultural Homogeneity) IQ test (Williams, 1972). What was found was that blacks scored highly, whereas whites lagged behind. But, the thing is, this test has ridiculous concepts that don’t test actual intelligence. The way that people say that regular IQ tests are biased towards blacks don’t even realize that the way the B.I.T.C.H. IQ test is set up does not mirror the supposed biased nature of regular IQ tests on blacks.

Flynn noticed that no matter which country you look IQs have gained around 3 points per decade. Herrnstein and Murray then coined the term The Flynn Effect, after the man who focused the most attention on the phenomena. Flynn argues that since IQ scores have been gaining the same amount of points in any population no matter where you look, that the black-white IQ gap has to be environmental in origin.

However, the Flynn Effect is a fallacy and is overstated. In 1945, the average IQ of whites in America was 85, the same as the black average today. That statement is supposed to show that the between-group differences are environmental in origin and since there haven’t been any big genetic changes in both populations to account for this difference, then the gap must be environmental in origin. Just because a change in one group over time is due to an environmental change, doesn’t mean, or even make it probable, that a difference between 2 groups at the same time is due to an environmental change. The Flynn Effect make’s that highly unlikely and here’s why.

Any country you look at, the rate of increase is 3 IQ points per decade; but gaps in IQ stay the same. This shows that this same uniform factor affects all groups the same throughout the world. And due to this uniform factor, as a result, you have a difference in IQ that’s being preserved. This suggests that the response on the parts of blacks and whites is due to non-environment factors, a genetic factor, which makes the difference in IQ remain as the Flynn Effect goes into effect.

Blacks and whites also have a similar environment, especially since segregation ended. Since environments are similar, the more and more similar the environment, the less and less differences are due to environment and the more and more they are due to genetic factors. So the 15-point gap surviving this change in environments proves that the racial gap is genetic in origin.

Dickens and Flynn state that black Americans have closed the gap in recent years, but this, however, is not the case. Most of those studies were done on children; Jensen states that the black-white IQ gap becomes more noticeable as they get older because genetic effects take over at adulthood with the environment having little if no effect on IQ (Rushton and Jensen, 2005). Jensen concludes that the SD gap between blacks and whites at early adulthood is about 1.2 SDs or about 17 IQ points. In Rushton and Jensen’s 2005 paper, Flynn and Dickens sidestepped a theoretical analysis in which it’s showed that the higher amount of white admixture a black has, the higher his IQ score is.

The Flynn Effect is not on g, or the general intelligence factor, which the most heritable items on the subtests show the most differences between blacks and whites (Rushton and Jensen, 2010). Since the Flynn Effect does not fall on g, this should not even be in the discussion. A Flynn Effect is not a Jensen Effect, which is real gains in over time (Rushton, 1998). Rushton found it ridiculous that we had a nation of mentally handicapped children 100 years ago. This was enough for him to disregard the Flynn Effect.

Other proposed causes for this gap involve a mechanism called ‘stereotype threat’ (Steele and Aronson, 1995). Stereotype threat is a situational predicament in which people find themselves falling into the stereotype of whatever group their group is a part of. Though, this is not the case for blacks. Blacks are rated as seeing themselves as more attractive, which a) shows more self-confidence and b) shows that the so-called effects of white racism making blacks feel ugly and inadequate in their own skin are simply not true. Kanazawa (2011) noted that both male and female blacks rated themselves higher than other groups; showing that there are no lingering effects of racism as well as this silly belief that just by thinking you’re going to fall into a stereotype means that you will fall into it.

Still, others may state that poverty is a cause for the IQ disparity between the races. People have causalities mixed up when they make this statement. Since lower IQ is correlated with lower SES, the cause of poverty is people being born with low intellect which manifests itself in the wealth attainment of the individual. Many recent studies have come out saying that poverty decreases IQ, yet the only environmental factors that can do such a thing is malnutrition, extreme abuse, and extreme isolation. Other than that, all a parent needs to do is just give the child an ‘OK’ environment and genetic factors will take care of the rest.

Critics of the public school system have said for decades that you can’t solve educational problems by throwing money at them, but those who believed in the public schooling system said it has yet to be tried. They did try, in Kansas, MO, and failed miserably (Ciotti, 1998). This desegregation experiment cost 11,700 dollars per student, more money spent per individual on a cost of living basis than 280 school districts around the country. This tax-payer money bought “higher teachers’ salaries, 15 new schools, and such amenities as an Olympic-sized swimming pool with an underwater viewing room, television and animation studios, a robotics lab, a 25-acre wildlife sanctuary, a zoo, a model United Nations with simultaneous translation capability, and field trips to Mexico and Senegal. The student-teacher ratio was 12 or 13 to 1, the lowest of any major school district in the country.”

Despite all of these variables to enrich the environment of the black students, even bussing in white kids from out of district, the gap did not diminish, test scores did not change and there was less, not more, integration. Moreover, numerous individuals say that poverty and schooling systems are the cause for anti-intellectualism in the black community. I, however, argue that there is a considerable genetic component to the black-white IQ gap (Rushton and Jensen, 2005 p. 279).

Where does all of this leave us? Yes, blacks are less intelligent than whites, but what does this mean for our society that we refuse to acknowledge the existence of innate intelligence, as well as racial differences in intelligence? The average IQ of a repeat juvenile criminal in America is 92 (Herrnstein, Murray, and Cullens, 1998). At adulthood, the average IQ for a repeat criminal is 85. The reason for the IQ of a repeat adult offender being lower than that of teenaged offenders is due to as you age, the environment doesn’t matter as genetics takes over at adulthood.

The fact that we are disregarding (intelligence) and its multiple covariates is extremely alarming. The fact that America is headed down the path to dysgenesis (Lynn, 2006) and we are not doing a thing about it troubles me greatly. The way we treat black underachievement in America is completely wrong. To succeed as a country, we need to recognize biological truths in that certain groups achieve highly whereas others have low levels of academic achievement, we need to recognize that there is no insidious plot to hold down others; we need to realize that some groups are less intelligent as others due to evolution in differing climates over tens of thousands of years. The trillions of dollars we have spent on all of these programs have not worked. We have tried them, and they have failed. No matter what we do, black underachievement will always be around. By recognizing black underachievement, they will be better able to succeed relative to themselves and not compare themselves to other high-achieving groups. There is a considerable genetic component to the gap (80 percent genetic) and that due to this, blacks should have differing standards in comparison to the rest of the population (Jensen, 1969).

References

Ciotti, P. (1998) Money and School Performance: Lessons from The Kansas City Desegregation Experiment   http://www.cato.org/pubs/pas/pa-298.html

Cullens, F.T., Herrnstein, R., Murray, C. Does IQ Significantly Contribute to Crime? (From Taking Sides: Clashing Views on Controversial Issues in Crime and Criminology, Fifth Edition, P 30-51, 1998, Richard C. Monk, ed. — See NCJ-183062)

Dickens, W. T., & Flynn, J. R. (2006). Black Americans Reduce the Racial IQ Gap: Evidence From Standardization Samples. Psychological Science, 17(10), 913-920. doi:10.1111/j.1467-9280.2006.01802.x

Duke, D.E. (1998). My awakening A path to racial understanding. Covington, LA: Free Speech Press.

Eriksen, H. F., Kesmodel, U. S., Underbjerg, M., Kilburn, T. R., Bertrand, J., & Mortensen, E. L. (2013). Predictors of Intelligence at the Age of 5: Family, Pregnancy and Birth Characteristics, Postnatal Influences, and Postnatal Growth. PLoS ONE, 8(11).

Eyferth, K. (1961). Leistungen verscheidener Gruppen von Besatzungskindern in Hamburg-Wechsler Intelligenztest fu¨r Kinder (HAWIK) [Achievement of children on the Hamburg-Wechsler Intelligence Scale for Children]. Archiv fu¨r die gesamte Psychologie, 113, 222–241.

Flynn, J. R. (1987). Massive IQ gains in 14 nations: What IQ tests really measure. Psychological Bulletin, 101, 171–191.

Gottfredson, Linda S. “Mainstream science on intelligence: An editorial with 52 signatories, history, and bibliography.” Intelligence 24.1 (1997): 13-23.

Herrnstein, R. J., & Murray, C. A. (1994). The bell curve: Intelligence and class structure in American life. New York: Free Press.

Jensen, A. (1969). How Much Can We Boost IQ and Scholastic Achievement. Harvard Educational Review, 39(1), 1-123.

Jensen, A. R. (1998). The g factor: The science of mental ability. Westport, CT: Praeger.

Kanazawa, S. (2011). Why Are Black Women Less Physically Attractive Than Other Women? The Scientific Fundamentalist

Lynn, R. (1996) Dysgenics: Genetic Deterioration in Modern Populations, Human Evolution, Behavior and Intelligence Praeger, 1996

Moore, E. G. J. (1986). Family socialization and the IQ test performance of traditionally and transracially adopted Black children. Developmental Psychology, 22, 317–326.

Murray, C. (2014) Our Futile Efforts to Boost Children’s IQ  http://www.aei.org/publication/futile-efforts-boost-childrens-iq/

Rushton, J. P., & Jensen, A. R. (2005). Thirty years of research on race differences in cognitive ability. Psychology, Public Policy, and Law, 11(2), 235-294.

Rushton, J. P., & Jensen, A. R. (2010). The rise and fall of the Flynn Effect as a reason to expect a narrowing of the Black–White IQ gap☆. Intelligence, 38(2), 213-219. doi:10.1016/j.intell.2009.12.002

Steele, C. M., & Aronson, J. (1995). Stereotype threat and the intellectual test performance of African Americans. Journal of Personality and Social Psychology, 69(5), 797-811. doi:10.1037/0022-3514.69.5.797

Tizard, B. (1974, February 1). IQ and race. Nature, 247, 316.

Weinberg, R. A., Scarr, S., & Waldman, I. D. (1992). The Minnesota transracial adoption study: A follow-up of IQ test performance at adolescence. Intelligence, 16(1), 117-135.

Williams, Robert L. (1972) The BITCH-100: A Culture-Specific Test.

 

“Philosophers of Science” and Race/IQ

1500 words

“Philosophers of Science” attempt to stick their heads into the race/IQ debate to give their field more credence than it should get with the hard sciences. They use bad arguments like saying that “gene-environment interactions are widespread and hard to entangle” (Block, 1995), not knowing that identical twins reared apart grow up to be so similar (Rushton and Jensen, 2005, p. 279). The only time they should stick their heads in this debate is when they’re affirming that the methodology used to test IQ as well as racial differences in IQ are sound; otherwise, they do not have the training to assess this. Most “Philosophers of Science” defend claims that disintegrate when presented with the relevant scientific evidence (Sesarardic, 2000). I will be referencing this paper for the length of this article.

Half of the paper analyzes Lewontin’s argument to Jensen in which he uses his now famous “seed argument” in which he says you can take two seeds from the same heterogeneous population and plant them in rich and poor soil and “. . . as a result, the phenotypic differences within each of the two groups of plants will be 100 percent heritable, but the difference between the two groups will be entirely due to differences in two environments (zero heritability).” The fact of the matter is, this argument is parroted by “Philosophers of Science” when Jensen never made that argument.

Jensen then systemically dismantled every environmental argument with empirical evidence that they don’t hold up.

Other researchers then made accusations of “racism” the reason for Jensen’s overlooking of this. James Flynn, a big opponent of the hereditarian hypothesis and Rushton and Jensen in general, say that Jensen is not a “racist”. There is also something called the “X-Factor”, which is when phenotypic differences between two groups can be explained by an environmental factor that has no within-group variation at all, a 0 heritability. Racism, however, is a poor excuse for the “X-Factor”. Both Flynn and Jensen rule out discrimination as being the cause for the “X-Factor” as well.

Simply put, Jensen doesn’t make inferences that the black-white IQ gap is genetically based on one or a few variables on their own, but everything put together, that’s where the remaining evidence put. “Philosophers of Science” don’t understand heritability coefficients to be saying what they do; they wouldn’t be saying that if they knew how they worked.

Sesardic brings up how Block (1995) only mentions three pieces of empirical evidence: The “Flynn Effect”, “data about caste-like minorities”, and the small amount of genetic variation between races.

  1. The Flynn Effect happens uniformly in all populations at a rate of 3 points per decade but has slowed considerably. This increase began starting around 1880, coinciding with the industrial revolution. Better nutrition increased brain size in all populations, which lead to an increase in IQ. The Flynn Effect is not on g, so to make any claims that the differences in IQ between blacks and whites, or global differences in IQ for that matter, can be changed with more favoring towards environmentalist positions are not consistent with the scientific literature. In 1945, the average white IQ in America was 85, the same as the average American black IQ today. Since the differences in IQ have stayed consistent despite better nutrition in all groups, this proves that the gap is genetic in origin. Just because a change in one group over time is due to an environmental change, doesn’t mean, or even make it probable, that a difference between 2 groups at the same time is due to an environmental change. Since the Flynn Effect does not occur on g, it should be a non-factor.
  2. Minorities are only “caste-like” because differences in IQ are heritable, leading to racial disparities in social class differences. We can see when we match blacks, whites, and “Hispanics” for IQ (100), that some differences disappear, other differences decrease dramatically, and even blacks and “Hispanics” beat out whites in a couple of variables. Through multiple IQ tests averaged over time as well as seeing that test differences between races stay mostly the same, we can then make the inference, with all of the other evidence, that racial and ethnic differences in IQ are mostly genetic in origin with the environment having very little effect. To say that “racism” or “stereotype threat” has any bearing on these racial differences in IQ is laughable because 1) stereotype threat is only replicable in the lab and 2) racism as a variable does not exist in IQ testing.
  3. The small amount of genetic variation between races as an argument for the non-existence of race is meaningless. There are around 3 billion base pairs in the human genome. The human races differ on around .1 percent of the genome, or around 3 million base pairs. This is more than enough genetic difference to show phenotypic differences (obviously) as well as genotypic differences (again, obviously). Richard Dawkins in the Ancestor’s Tale writes: “What is not correct is the inferene that race is therefore a meaningless concept.” Race is a perfectly valid concept, anyone who denies it has doesn’t know of all of the studies that show the existence of race and how it’s a scientifically taxonomic concept.

Sesardic then brings up how “Philosophers of Science” continuously cite The Mismeasure of Man and Steven Jay Gould in an attempt to denigrate scientists long dead. A few “glowing reviews” from two “Philosophers of Science”:

No one has done as much as Stephen J. Gould to expose race and intelligence studies for the garbage that they often are. (Brown 1998, 5)

Stephen Jay Gould has lucidly analyzed how filling the skulls with lead shot, and comparing the weights of the lead, could easily be infected with unconscious biases. (Kitcher 1997, 171)

The garbage that they often are? Steven Jay Gould is a long discredited ideologue who put his politics before actual science, ironically giving HIM the same bias he falsely accused Samuel Morton of having. James Flynn even says that Gould’s book evades all of Jensen’s best arguments (as most always happens with this debate) with his false belief that is “reified” therefore leading to the study of race and IQ being meaningless since he has “rebutted the factor”. I proved the existence of Spearman’s hypothesis the other day using Jensen’s writings that he empirically verified that Spearman’s hypothesis exists in 25 independent samples of blacks and whites along with the study by Dragt (2010) who used the method of correlated vectors to empirically prove the existence of Spearman’s hypothesis. In meta-analyses of Spearman’s hypothesis, he found that differences in intelligence between groups are largely based on cognitive complexity and any so-called “biases in mental testing” cannot account for these racial differences in cognitive ability. 

In the definitive refutation of Steven Jay Gould’s “reanalysis” of Morton’s skulls, Lewis, et al definitively prove by remeasuring 308 of the 670 skulls that he had no implicit biases. They also found that if Morton’s biases were true, then there would be considerable overestimates of white skulls while there would be considerable underestiamates of non-white skulls. Ironincally enough, he considered his Egyptian skulls “Negroid” and overmeasured by 12 percent. He overmeasured three of those skulls, along with Seminole (by 8 percent) and native African Nergro (by 7 percent), falsifying the claim that Morton had a bias in measuring his skulls!! As I have brought up here numerous times, as Rushton has refuted him (and defended Morton’s results) as well as Jensen giving Gould a definitive rebuttal to his book. Gould should not be being cited seriously anymore. He should only be brought up as an example of extreme bias in the context of race as well as racial differences and a whole slew of other things that are politically motivated.

He finally rounds up the paper by bringing up how TJ Bouchard, showing that the Big Five Personality Traits have a high heritabilty, gets told that they are traits that carry a social judgment. However, we now know that 40-60 percent of the variation the Big Five is heritable, so this is a meaningless claim.

Sesardic ends the paper as follows:

Why is this small segment of contemporary philosophy of science in such a sorry state? On reflection, I prefer to leave this question as an exercise for the reader. My aim in this paper is to criticize a deviant philosophical trend, not to explain how it came about or why it spread.

My answer to this question is that most philosophers seem to be leftists. We can see with the vehement race denial that they want to believe so strongly that racial differences, as well as race as whole, does not exist. The fact that they attempt to say that these things are not a reality and based on faulty methodologies shows that they do not know what they are talking about. They show large misconceptions about heritability, and continuously cite Steven Jay Gould, even when Gould has been refuted numerous times as well it being shown that they don’t correctly understand heritability. They show large misconceptions of what is understood in the field of psychometrics and heritabilities and make faulty claims about the hereditarian hypothesis.

If the hereditarian hypothesis is to be refuted (it won’t), it will be from science and not philosophy or “Philosophers of Science”.

Science Daily: Mom’s Exposure to BPA During Pregnancy Can Put Her Baby on Course to Obesity

1750 words

Science Daily came out with an article today that exposure to BPA invitro for babies is correlated with obesity at age 7. 94 percent of the women tested had detectable levels of BPA. BPA is also linked with early onset puberty, which I will also speak on later in this article as it has implications for one of my theories.

I briefly touched on BPA in my article What’s the Cause of the Cucking of Europe? where I said:

I advise all of you (women included, there are many deleterious effects of BPA on the mother as well as the baby prenatally), to discontinue use of plastics with BPA in them.

The above-linked study shows that preeclampsia is correlated with elevated levels of BPA in the blood levels in the pregnant mothers, fetal blood, and the placenta. BPA was found to be elevated in mother’s fetal tissue with preeclampsia in comparison to the mothers with lower levels of BPA in their fetal tissue. I will come back to the BPA link with preeclampsia later in the article as it has implications for ethnic groups in America.

The paper, which was just released on the 17th, called Bisphenol A and Adiposity in an Inner-City Birth Cohortcarried out tested BPA in three differing subjects: 375 babies invitro, (3rd trimester) children aged 3 (n=408) and aged 5 (n=518) (Hoepner, et al, 2016). They measured the children’s bodies as well as measuring body fat levels with bioelectrical impedance scales.** Prenatal urinary BPA was positively associated with waist circumference as well as fat mass index, which was sex-specific. When analyzed separately, it was found that there were no associated outcomes in body fat for boys (however it does have an effect on testosterone), but there was for girls (this has to do with early onset puberty as well). They found that after controlling for SES and other environmental factors, they discovered that there was a positive correlation with fat mass index – a measure of body fat mass adjusted for height, body fat percentage and waist circumference. The researchers say that since there was no correlation between BPA and increased obesity, that prenatal exposure to BPA indicates greater vulnerability in that period.

The researchers then conclude that BPA exposure invitro “may be an important underlying factor in the obesity epidemic” and that “Endocrine disrupting chemicals like BPA may alter the baby’s metabolism and how fat cells are formed early in life.”

If true, this has huge implications for the way we look at the obesity epidemic in this country. Who are the most likely to be obese? “Hispanics” and blacks (Ogden et al, 2014).

Returning to what I brought up earlier about early onset puberty: in my article on the hormone leptin being a cause for earlier menarche in black girls, I noted that since black girls were more likely to be heavier as well as mature faster than white girls, that differences in leptin were the cause of differences in menarche between the two groups.  Elevated levels of serum leptin were correlated with body fat and differences in maturation between the two groups. Differences remained, but lessened, after controlling for differences in fat mass, maturation, age, and physical fitness.

Since BPA is correlated with adiposity in children and black girls have earlier menarche DUE to there being a higher chance of black girls being overweight in comparison to white girls, BPA is yet another piece to the puzzle of this phenomena, along with, of course, evolution. Ingestion of BPA is an environmental factor, however, with these changes in body chemistry in the children invitro due to increased BPA consumption by the pregnant mothers, it leads to one cause that can be prevented from further occurring due to our new knowledge.

The study was carried out on a cohort from NYC. In 2010 in NYC, the city was: 44 percent white, 25.5 percent black, 12.7 percent Asian with the rest being filled out by ‘Hispanics’ (not a racial category) and mixed-race people. Even after they matched for SES and other environmental factors, these differences persisted. However, this study was only carried out on those women who self-identified as either Dominican (basically African) and black. To quote the researchers:

Women were included if they self-identified as either African American or Dominican and had resided in Northern Manhattan or the South Bronx for at least 1 year before pregnancy. Exclusion criteria included mother’s report of: cigarette smoking or use of other tobacco products during pregnancy, illicit drug use, diabetes, hypertension, known HIV, or a first prenatal visit after the 20th week of gestation.

So, we have a full sample of Caribbean Africans and African Americans in this study. What else can we learn about those two populations and their consumption of things with BPA in them?

race differences tap and bottled water

The above Figure (7) is taken from the U.S. Department of Agriculture and the Food Surveys Research Group study on differences in drinking tap and bottled water.in different populations in the country. As you can see in this figure (what is notable is the ages 12-19 and 20 to 60 in the table), whites at all age groups drink more tap water. Blacks and ‘Hispanics’ were pretty much even in consumption of bottled water. However, Mexican American girls, like black girls, are also entering puberty earlier. Since both populations have a substantial percentage of them overweight and obese (factor for serum leptin production which then causes early onset puberty), this again shows a strong correlation between body fat gain and early onset puberty. Moreover, this also shows that both Dominican and black populations consume more bottled water than do white populations, both populations are more likely to be obese or overweight (even after controlling for SES) which causes leptin production earlier causing periods to happen much sooner than in populations who drink less bottled water and use other products with BPA in them. .

Going back to preeclampsia, it is a condition that pregnant women develop that’s characterized by hypertension (high blood pressure) and protein in the urine. It’s known that black women suffer from it the most. More interestingly, over the past ten years, rates of preeclampsia have been increasing in the black female population. As the researchers note in the article, BPA is correlated with preeclampsia. Blacks have a higher rate and chance of being diagnosed with hypertension as well. All of these differing variables coalesce into our current obesity epidemic. With blacks and “Hispanics” being more likely to be overweight/obese drink more bottled water, have a higher risk for hypertension, higher risk for preeclampsia and having earlier menarche, these help explain, in part, racial/ethnic differences in obesity.

These differences can be attributed to consumption of bottled water, i.e., consuming things with made with and packaged in plastic as well as canned foods. From my experience with Dominican and black New Yorkers, they tend to have horrible lifestyles, tend to drink tons of bottled water and also tend to be overweight or obese at a higher rate in comparison to the general population. This leads to biologic factors changing (i.e., earlier menarche in younger girls) in these young girls, leading to devastating effects on their body chemistry.

This study, yet again, proves another underlying factor for obesity in certain populations in the country. And what do you know? It’s the populations that already have the highest rate of obesity in the country. When it becomes definitive that BPA consumption by pregnant mothers does lead to underlying factors in obesity. To quote the researchers: “Endocrine disrupting chemicals like BPA may alter the baby’s metabolism and how fat cells are formed early in life.” This will be HUGE for our understanding of underlying causes to obesity! Moreover, if (when) this is fully corroborated, it can then be said that by mothers exposing their children in the womb to excess levels of BPA, there is a chance that they are “giving their own choice to make their children have a higher chance of being obese, as they know the dangers of BPA consumption during pregnancy and all of the negative variables associated with it.”

This is an extremely interesting and important study for our understanding of obesity. Since BPA consumption invitro is correlated with higher fat mass index in girls at age 7, and since those girls who tend to be more overweight and obese than other populations, we can then say that BPA has a hand in obesity in children, which then causes serum leptin to be released, causing way menarche in these populations. An increase in sexual maturation has been linked to the obesity epidemic, which began around 60 years ago. The cause of this is due to the demonization of the fat macro and carbohydrates, all the while it was reversed. This destroyed insulin sensitivity for many Americans, leading to a huge majority of our health problems today.

In conclusion, underlying factors for obesity keep appearing. Due to racial/ethnic differences in bottled water consumption (one of the most common BPA products in households), which the effects of BPA may alter how fat cells are formed in early life, this accounts for, in part, excess adiposity in differing populations. These underlying factors could help show where some of these racial/ethnic differences in obesity come from. Since the two populations in the study (black American and Dominican) both have high levels of adiposity, both drink a lot of bottled water and both have earlier menarche than do whites (who drink LESS bottled water), this shows that some (a lot?) of the variation in obesity between ethnic/racial groupings can be explained by these underlying factors.

** I have one problem with this study. They assessed fat mass index with bioelectrical impedance.The machine sends a light electrical current through the body and measures the degree of resistance to the flow of the current, which body fat can then be estimated. Problems with measuring body fat this way are as follows: it depends on how hydrated you are, whether you exercised that day, when you last ate, even whether your feet are calloused. Most importantly, they vary depending on the machine as well. Two differing machines will give two differing estimates. This is my only problem with the study. I would like if, in a follow-up study, they would use the DXA scan or hydrostatic weighing. These two techniques would be much better than using bioelectrical impedance, as the variables that prevent bioelectrical impedance from being a good way to measure body fat don’t exist with the DXA scan or hydrostatic weighing.